Previous studies from our laboratory have implicated a population of activated suppressor lymphocytes which produce an inhibitory lymphokine as pathogenic in patients with bone marrow failure. These cells are detectable in abnormally high numbers in the circulation of patients with aplastic anemia. Production of gamma interferon by activated suppressor cells probably explains other laboratories' previous results showing inhibition in co-culture by patients' cells of normal hematopoiesis. Current studies have been directed at the changes in lymphocyte phenotypes and lymphokine production in patients that follow treatment with antithymocyte globulin (ATG); the mechanism of action of ATG in aplastic anemia; and the interaction in vitro of gamma interferon with other soluble mediators of immune function. The scope of studies of aplastic anemia has been broadened by collaborations with investigators in the Far East, where aplastic anemia is a more common disorder than in the United States or Western Europe.